Download Chronic hepatitis D

HEPATITIS D
Dr.Hamid Ghorbani
M.D.Infectious disease specialist
Mashhad, khorasan razavi , Iran
HEPATITIS DELTA VIRUS
Delta agent was identified by Mario Rizzetto in 1977 as a
nuclear antigen distinct from HBsAg, HBcAg, and HBeAg in
hepatocytes of some HBsAg carriers in Italy.
It soon became clear that this passenger virus, termed
hepatitis D virus (HDV), accompanied HBV infection and
required the HBsAg for transmission.
This unique HDV RNA genome resembles plant
pathogens. HDV is the only member of the genus
Deltavirus.
In nature, HDV is only found in patients who are also
infected with HBV,woodchucks and Chimpanzees.
Hepatitis D infection
Epidemiology
Prevalence in iran
• The pooled HDV prevalence was 7.8%
(95% CI: 5.89 - 9.71).
• The prevalence of HDV is less common in
Iran than in endemic regions such as Italy
and Turkey.
• The most probable route of HDV
transmission is hematologic.
Prevalence in Mashhad
• -prevalence in chronic hepatitis B
patients:10%
• prevalence in chronic hepatitis B patients
with chronic liver disease and
cirrhosis:14.2%
• Risk factors:1-transfusion 2-positive family
history
Pathogenesis
• HDAg is the only viral protein known to be expressed during HDV
• infection.
• A high titer of IgM anti-HDV is strongly associated with elevated
hepatitis D viremia and the severity of liver injury, whereas a more
favorable course to HDV infection is found in individuals with IgG
anti-HDV.
• There is no convincing evidence of a protective role of anti-HDV
antibodies.
• The mechanisms of liver damage in HDV infection are unclear.
•
The adaptive immune response plays an important role in
pathogenesis and control of HDV infection, but the precise
• mechanisms are unknown.
• The presence of HDV-specific T-cell responses correlates with lower
• ALT levels, suggesting that immune control of viral replication leads
• to lesser degrees of liver injury.
• The immune response contributes to hepatocellular injury.
Clinical
Manifestations
• HDV is spread by blood, blood products,
and bodily secretions similar to HBV.
• Following exposure, there is a short
incubation period of 3 to 7 weeks.
Acute coinfection with HBV
• 1- biphasic pattern of ALT levels : Usually the first episode
• is due to hepatitis B replication and immune response, followed by
that of hepatitis D.
• 2-An acute self-limited hepatitis with complete recovery, similar to
other viral hepatitis infections, and chronic infection is seen in only
2%.
• 3-severe or fulminant hepatitis is rare.
Acute superinfection with HBV
• 1-Severe hepatitis
• 2-Short incubation period
• 3-Chronic hepatitis D in 90% of the cases.
• 4-Fulminant hepatitis and chronic active hepatitis with cirrhosis.
Fulminant hepatitis,is 10 times more common in coinfection.
•
In patients with chronic HDV, HDV is the dominant virus because it
suppresses HBV replication. Thus, most HBV-HDV coinfected
patients have low serum HBV DNA levels.
Chronic hepatitis D
• 1-Clinical course of hepatitis is accelerated.
• 2- Cirrhosis occurs in 60% to 80% of chronic hepatitis D
patients, and the risk of HCC is about threefold.
• 3- Splenomegaly along with elevated transaminases and
high levels of viremia are common.
•
• 4-Unlike HBV, the level of HDV viremia does not seem to
correlate with severity of disease.
HIV-HBV-HDV triple infection
• 1-Liver disease is known to be accelerated
• The incidence of HCC and mortality is
higher than in patients with HIV alone.
Treatment options
Choice of therapy
IFN- alfa